"...Normally, these old cells are cleared by the body, but the process becomes less efficient with age. So researchers at the Mayo Clinic used a drug to target only senescent cells and force them to self-destruct, in a group of mice that were genetically engineered to age rapidly.

"In mice that were treated throughout their lifetimes, researchers said they saw a remarkable delay in the development of cataracts, muscle wasting and the type of fat loss that, in humans, causes skin wrinkling. Another group of mice was treated in older age, after cataracts had already set in. The drug didn't reverse the age-related changes that had already occurred, but it prevented further decline."

Comment: This study seems to suggest that cataractognesis is part of the aging process and that a certain drug is capable of targeting the underlying inflammatory factors [as indicated in the original article]. This is odd, the nucleus of the crystalline lens contains the oldest cells in the body and aggregation of the crystallins causes nuclear cataracts - not some inflammatory process. Even if so, how would the drug enter the lens, through the cortex and force the tightly packed, senescent nuclear lens fibers to self-destruct only to leave a huge central vacuole behind?